There’s been a recurrent trending topic in the scientific community’s Twitter feed in the last week or so – the increasing problem of antibiotic resistance and in particular, the isolation of a new superbug gene that could be coming to a hospital near you very soon. But what are these so-called superbugs, how did they get here, and how are we going to stop them?
Superbugs are, in short, strains of bacteria that have evolved the ability to be unaffected by antibiotics – the drugs that we use to kill them and prevent the spread of infection. The superbug that most people are most familiar with is MRSA. This stands for “methicillin-resistant Staphylococcus aureus”. Staphylococcus aureus is a very common bacterium that is often found living happily on our skin and up our noses without giving us any grief. It usually only causes problems if it gets somewhere that it shouldn’t be, like into a wound, and if that happens, a trip to the GP and a course of penicillin will usually see you right. MRSA however is a strain of this normally docile bacterium that doesn’t die when treated with bog standard antibiotics, or even with some of the more expensive ones that you might be given if you were in hospital with a more serious infection.
Superbugs evolve in the same way that any organism evolves – through the Darwinian process of natural selection, leading to “survival of the fittest”. The difference with bacteria however, is that bacteria don’t just reproduce sexually or asexually like the majority of other organisms – they also have a weird and wonderful way of sharing and swapping genes with other bacterial cells, simply by passing them through the cell membrane as they float past. As well as this, they reproduce so darn quickly – doubling in numbers every few minutes or hours – that natural selection takes place on an accelerated scale. Compare this with the 5 or 10 years that it takes scientists to identify and process new drugs through clinical trials to the open market, and it’s no wonder that our antibiotics are getting out of date.
The thing that’s been getting the scientific community in a tizzy lately is the fact that bacteria carrying a gene that gives antibiotic resistance against a group of antibiotics called carbapenems has been found in the drinking water supplies of the Indian city New Delhi (The Lancet Infectious Diseases (11)70059-7, 2011). The gene, NDM-1, has the ability to transfer into several different bacterial strains, which means that it is likely to spread very quickly, and carbapenems are used to treat the most serious and stubborn, hard-to-treat infections. Thanks to the large amount of international travel to and from India, NDM-1 has already found its way to the UK and healthcare providers are bracing themselves for a crisis.
So what can we do about antibiotic resistance? Well, firstly, we need to stop using antibiotics as a cure-all for the slightest of infections. We humans are just a little bit antibiotic-mad and the fact that Fleming’s wonder-drugs have traditionally been so effective means that we’re happy to pop pills for all manner of small, non-urgent infections, especially in those countries where strong antibiotics can be bought over the counter without a prescription.
Secondly, we need to embrace organic farming and put an end to the practice of feeding our livestock with antibiotics in order to produce bigger and fatter animals for meat. In any battle, if you try the same tactic too many times, the enemy will eventually get wise to it and beat you at your own game. So it is with bacteria. By bombarding our animals with the same varieties of antibiotics over and over again – often needlessly – bacteria are now becoming more and more able to evade our weapons. In fact, a recent study published in BioMed Central’s very own BMC Environmental Health found that flies and cockroaches living in pig poo were an important vector in the transmission of antibiotic resistant bacteria from animals to humans.
Thirdly, we need to stay healthy. Obviously this is easier said than done, but most serious infections with antibiotic resistant bacteria occur in hospitals – not necessarily because hospitals are germ-ridden, but because when we’re in hospital, we’re often immunosuppressed. When our immune systems are weakened, bacteria can take hold and our natural defences are less able to cope, resulting in infections that spread rapidly and can overwhelm us.
Lastly, of course, we need new antibiotics, and new, faster approaches to antibiotic development. A Taiwanese group of researchers have recently published findings in Nature Chemical Biology that demonstrate the potential for tweaking the chemical structure of existing antibiotics in order to improve efficacy. Results have been promising in the Petri dish and rat models, but further tests and trials will need to be done before these drugs can be developed for human use. The question is, will it be too late by then?